The utility of cardiovascular imaging in heart failure with preserved ejection fraction: diagnosis, biological classification and risk stratification

Figures

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  Fig. 1. Echocardiographic measures used to assess diastolic dysfunction. a Mitral valve (MV) E-wave and A-wave peak velocities, obtained on pulse-wave Doppler, are combined to generate the E/A ratio. b Mitral valve E-wave peak velocity and tissue Doppler (TDI) eʹ velocity (here measured at the lateral MV annulus; average eʹ is calculated from both the lateral and medial sites) are combined to generate the E/eʹ ratio. c Peak velocity of tricuspid valve (TV) regurgitation. d Apical 2-chamber view and measurement of left atrial (LA) volume. DT–deceleration time

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  Fig. 2. Speckle-tracking measures on echocardiography. a Peak apical rotation and untwist measurements from the apical short-axis view (SHAX). b Basal rotation and apical rotation generates peak left ventricular (LV) twist, measured from the basal-SHAX and apical-SHAX, respectively. c Peak LV untwisting rate, measured from the apical-SHAX. d Peak global longitudinal strain rate during isovolumetric relaxation (SRIVR). e Left atrial (LA) strain in the apical 4-chamber view measured as reservoir, conduit, and booster strain. AVC–aortic valve closure; MVO–mitral valve opening

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  Fig. 3. Specific causes of heart failure with preserved ejection fraction (HFpEF) diagnosed on cardiac magnetic resonance imaging (CMR). a Short axis late-gadolinium enhancement (LGE) sequence in a patient with HFpEF secondary to cardiac amyloidosis. Diffuse subendocardial enhancement is seen in the left and right ventricles. b Apical 4-chamber view in the same patient showing subendocardial LGE. c Apical 4-chamber cine in a patient initially diagnosed with ‘HFpEF’. Increased wall thickening and hypertrophy are seen at the left ventricular (LV) apex typical of apical hypertrophic cardiomyopathy. d Short axis cine in a patient presenting with ‘HFpEF’, demonstrating pericardial thickening and ‘D’ shaped flattening of the septum towards the LV during diastole. Subsequently diagnosed with pericardial constriction

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  Fig. 4. Myocardial fibrosis assessed by T1-mapping and extracellular volume (ECV). a Native T1 map of the basal left ventricle (native T1 time 1021 ms). b Post-contrast T1 map (post-contrast T1 time 432 ms). c ECV map (calculated ECV 32.6%)

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  Fig. 5. Myocardial energetics assessed by 31phosphorous-magnetic resonance spectroscopy (31P-MRS). A chemical-shift imaging 31P-MRS sequence, with voxel grid aligned to the ventricular septum, generates a frequency spectrum denoting phosphocreatine (PCr), γ-, α- and β-adenosine triphosphate (ATP), thus calculating the PCr to ATP ratio

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  Fig. 6. Cardiac magnetic resonance imaging (CMR) measures of arterial stiffness. a–d Pulse wave velocity (PWV) is calculated between the ascending and descending aorta by the transit-time method. A Aortic ‘candy-stick’ cine is used to plan a through-plane velocity flow map, demonstrated by the green line bisecting the pulmonary artery. The aortic distance between the two aortic locations is measured (∆x). b, c Through-plane flow and magnitude images generated from the aortic candy stick. The ascending aorta is contoured in Red and the descending aorta in Green. d Graph demonstrating flow in the ascending aorta (Red) and descending aorta (Green) during systole. Time to half the peak flow rate is measured and the difference calculated as the transit time (∆t). PWV is calculated by the equation PWV = ∆x/∆t. e, f Through-plane cine image of the ascending aorta. The maximal (e) and minimal (f) aortic areas through the cardiac cycle are calculated. Ascending aortic distensibility (AAD) is calculated by the equation AAD = ∆A / (Amin × PP), where ∆A represents the change in aortic area, Amin the minimal aortic area, and PP the pulse pressure